@jpring
Long story short, withdrawing from benzodiazepines can be a pain in the ass too, and is known to cause tinnitus if you do it too quickly. I'm guessing that's what happened to you, but in a similar way to benzos. You stopped drinking suddenly, and your central nervous system is used to have all that depressant ethanol hanging around. As a result, your central nervous system then goes into overdrive in the absence of the depressing agent. .
yes, cns overdrive is a common cause, whether from chemical withdrawal,prolonged stress or sudden shock.
seems the brain seeks out potential threats, breaches filters, zones in on neuronal activity, unmasks tinnitus.
Maybe the brain zones in on frequencies where the brain has been receiving less auditory input, especially where there are notches, which would signify greater danger areas ("hey, we can't hear predators at 4khz"), who knows.
Up to that point you may or may not have had significant hearing loss, but you will have had hearing loss because that's part of ageing. noone's got technically perfect hearing and some people have deeper troughs.
And as Dan points out, your real hearing goes way above normal hearing tests which are therefore not too helpful if your problems lie upstream.
Just curious but maybe there are different types of tinnitus.
Firstly, where a shocked CNS sends the brain into hyper-vigilance, busting its way through thalamic perception filters to unveil previously cloaked brain sounds. (from my experience, distraction/de-attention helps rebuild those filters)
Secondly, where acoustic shock results in DCN neurons becoming over-active. Big populations of neurons acting in synch. This has been the target of therapies like coordinated reset stimulation, etc. Over-activity looks like a hot target when you consider that tinnitus has been suppressed by electrical stimulation of the auditory nerve using cochlear implants (chang 2012). Maybe residual inhibition works like this too when you consider sound is converted by your ears into electrical impulses. Hopefully resounding success will come from smart drug Autifony, which has already shown amazing success targetting these neurons via potassium channels.
Could someone tell me how these two 'types' are linked. Are they part of the same picture?
In the first scenario, we have existing brain sounds unveiled, maybe not over-active neurons.
In the second scenario, we have sound damage sending neurons into definite over-spin.
And how does this fit in with discordant dysfunction theory (imbalance between inner and outer hair cells)
Is such a theory now defunct or irrelevant in light of what Autifony offers?
I really understand very little about the brain, so we'd all welcome a mini-lecture from anyone here who can enlighten us, especially on the full mechanism of Autifony. I want to believe that both scenarios create hyper-active neurons that can be tackled by Autifony so we can all go home and get some decent sleep!
Wishing jpring and all of us wellness soon.
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